Impaired neural conduction in crossed visual pathways in patients with ocular hypertension.

PURPOSE: To evaluate the neural conduction along crossed and uncrossed visual pathways in patients with ocular hypertension (OHT). METHODS: Fifteen patients (mean age 59.1+/-6.8 years) with OHT (IOP>22 mmHg, Humphrey 24-2 with mean deviation [MD]>-2 dB) were enrolled. They were compared to 15 age-matched controls. In OHT patients and control subjects, visual evoked potentials (VEPs) were recorded using full-field checkerboard patterns (the check subtended 15' of visual arc; contrast 80%) reversed at 2 Hz. VEP responses were simultaneously recorded in the homolateral visual cortex (HC) and in the contralateral visual cortex (CC), with respect to the stimulated eye. RESULTS: In OHT patients, VEP P100 implicit times observed in HC and CC were both significantly delayed (analysis of variance, p<0.01) when compared to those of controls, and, in particular, longer in CC than in HC. The interhemispheric differences (ID: P100 implicit time in HC - P100 implicit time in CC) were significantly higher in OHT patients than controls (-3.16+/-1.80 msec and 1.16+/-1.04 msec, respectively, p=0.001). In OHT patients we observed an MD hemifield difference (difference between nasal and temporal MD values) higher than in controls (-0.82+/-0.80 dB and 0.04+/-1.03 dB, respectively, p<0.01) and significantly correlated with the ID (r: 0.836, p<0.001). CONCLUSIONS: The observed asymmetry in the bioelectrical cortical responses and in the visual hemifield parameters suggests that crossed visual pathways could be impaired earlier than uncrossed visual pathways in OHT patients.

Neurotrophic keratitis.

Neurotrophic keratopathy is a degenerative corneal disease induced by an impairment of trigeminal nerve. Impairment of loss of corneal sensory innervation is responsible for corneal epithelial defects, ulcer, and perforation. In the present report, we reviewed the pathogenesis, diagnosis, and therapeutic aspects of this disease. An accurate history and clinical examination, including the function of cranial nerves, together with the clinical features of the ocular surface are essential for a prompt diagnosis. The evaluation of the corneal sensitivity and tear film function are important diagnostic steps as well. Specific medical and surgical treatments, based on the clinical staging of the disease, are often able to halt its progression. Future developments in the medical treatment including the administration of neuropeptide and growth factors are presented.

Correlation between optical coherence tomography, pattern electroretinogram, and visual evoked potentials in open-angle glaucoma patients.

OBJECTIVE: [corrected] To correlate the nerve fiber layer (NFL) thickness and the visual function evaluated by electrophysiologic retinal and cortical responses assessed in open-angle glaucoma (OAG) eyes. DESIGN: Prospective case-control study. PARTICIPANTS: Thirty glaucoma patients (mean age, 47.1 +/- 7.15 years; refractive error range, +/- 2 spherical equivalent) with a mean deviation of computerized static perimetry (24/2 Humphrey, Dublin, CA) from -5 to -28 dB and intraocular pressure less than 21 mmHg on pharmacologic treatment and 14 age-matched control participants. METHODS: Nerve fiber layer thickness was measured by optical coherence tomography. Retinal and visual pathway function was assessed by simultaneously recording pattern electroretinograms (PERGs) and visual evoked potentials (VEPs) using high-contrast (80%) checkerboard stimuli (the single check edges subtend 15 minutes of the visual arc) reversed at the rate of two reversals per second. Linear regression analyses were adopted to establish the correlation between NFL thickness and PERG and VEP parameters. MAIN OUTCOME MEASURES: Nerve fiber layer thickness measurements in each quadrant (superior, inferior, nasal, and temporal) were taken and then averaged (12 values averaged) and identified as NFL overall, whereas the data obtained in the temporal quadrant only (three values averaged) were identified as NFL temporal. PERG P50 implicit time and P50-N95 amplitude and VEP P100 implicit time and N75-P100 amplitude were also measured. RESULTS: In OAG eyes, we found a significant (P < 0.01) reduction in NFL thickness in both NFL overall and NFL temporal evaluations with respect to the values observed in control eyes. PERG and VEP parameters showed a significant (P < 0.01) delay in implicit time and a reduction in peak-to-peak amplitude. In OAG eyes, the NFL overall and NFL temporal values were significantly correlated (P < 0.01) with the PERG P50 implicit time and P50-95 peak-to-peak amplitude. No correlations (P > 0.01) between NFL values and VEP parameters were found. CONCLUSIONS: There is a correlation between PERG changes and NFL thickness, but there is no correlation between VEP changes and NFL thickness in patients affected by OAG.

Visual electrophysiological responses in subjects with cerebral autosomal arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL).

OBJECTIVES: To evaluate visual electrophysiological responses in subjects with cerebral autosomal arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). METHODS: Three subjects (one male and two females, mean age 55.3+/-2.9 years) belonging to an Italian family already diagnosed with CADASIL through clinicopathological and genetic studies and 14 control subjects (6 males and 8 females, mean age 52.7+/-3.6 years) were enrolled in the study. Flash electroretinogram (ERG), oscillatory potentials (OPs) and simultaneous recordings of pattern electroretinogram (PERG) and visual evoked potentials (VEPs) were assessed in all 3 subjects with CADASIL and age-matched controls. RESULTS: Subjects with CADASIL showed: reduced ERG, OP and PERG (N35-P50, P50-N95) amplitudes with respect to our normal limits; delayed PERG (N35, P50) and VEP (P100) implicit times when compared with our normal limits; and VEP (N75-P100) amplitudes and retinocortical times within our normal limits. CONCLUSIONS: Subjects with CADASIL present a dysfunction in the outer, middle and innermost retinal layers when the index of neural conduction in the postretinal visual pathways is normal. The delay in visual cortical responses observed in subjects with CADASIL may be ascribable to retinal impairment with a possible functional sparing of the postretinal visual structures.